Hormonal and Metabolic Changes following Severe Head Injury or Noncranial Injury

Abstract

In order to evaluate the effect of head injury in severely traumatized patients on the response of plasma cortisol, glucagon, insulin, glucose, and FFA as well as urinary N and catecholamines excretions, 36 patients were prospectively studied over 5 consecutive days following injury. They were divided into three groups: group I, severe isolated head injury (n = 14); group II, multiple injury combined with severe head injury (n = 12); group III multiple injury without head injury (n = 10). The results demonstrate similar hormonal and metabolic changes between these three groups of patients, characterized by elevated urinary adrenaline, noradrenaline excretion, increased cortisol, glucagon, insulin plasma levels throughout the study and elevated N urinary excretion with strongly negative N balances during the first 5 days postinjury. A significant correlation was observed between N intake and 5 day cumulated N balance (r = 0.63, p less than 0.001). In addition, N balance was negatively correlated with urinary excretion of adrenaline (r = -0.47, p less than 0.01) and noradrenaline (r = -0.44, p less than 0.05) as well as plasma levels of glucagon (r = -0.44, p less than 0.05). Isolated severe head injury seems to induce a full response in the secretion of the catabolic counterregulatory hormones comparable to that encountered in patients with multiple injury and associated with a marked increase in protein catabolism; additional noncranial major injury does not seem to enhance these responses.

Plasma glucose level in Nigerian Africans with head injury

“…These have been confirmed. 8,10 The reason for the discrepancy between our results and other reports is not clear. These reports were conducted in predominantly white populations and in more developed countries; could there be a racial difference in the metabolic response to trauma?…”

“…The increase in these hormones has been confirmed. [8][9][10] The severity and outcome of head injury is related to the degree of hyperglycemia; severe injury and poor outcome are associated with high glucose concentrations. 1,2,[5][6][7]11,12 Values of serum glucose of 200 mg/dL (11.1 mmol/L) have been related to poor outcome.…”

Hypermetabolism following Moderate to Severe Traumatic Acute Brain Injury: A Systematic Review

“…In one study, a portion of the metabolic measurements were obtained using a metabolic cart, which became available during the study's duration . Among the studies that used a metabolic cart, the sampling period varied from less than 30 min (Esper et al, 2006;Hadfield et al, 1992;Kolpek et al, 1989;Moore et al, 1989;Petersen et al, 1993;Young et al, 1985), to (Clifton et al, 1981;Dahlberg et al, 1985;Fell et al, 1984;Godbole et al, 1991;Kaufman et al, 1987;Nataloni et al, 1999;Stechmiller et al, 1994) 3 (Bivins et al, 1986Chiolero et al, 1989a;Fife and Jagger, 1984) Energy expenditure not compared with a predicted value 6 (Bucci et al., 1988;Deutschman et al, 1986;Feldman et al, 1993;Hatton et al, 1997;Hatton et al, 2006;Krakau et al, 2007) 3 ( Ott et al, 1999;Suchner et al, 1996;Waters et al, 1986 figure. (results from head-injured patients only reported)…”

“…Although our understanding of the etiology of this phenomenon is not complete, the release of various cytokines and counter-regulatory hormones, mediated through the acute phase response, is believed to be contributory (Chiolero et al, 1989a;Young et al, 1988Young et al, , 1992. Wide variations in both the magnitude and time course of metabolic perturbations have been reported, with energy expenditures ranging from 32% (Long et al, 1979) to 200% (Haider et al, 1975) above that which would be predicted in the non-injured state.…”

A resposta metabólica ao trauma cranioencefálico é autolimitada? Análise das proteínas de fase aguda e glicemia

“…É possível pressupor também que, uma eventual persistência da hiperglicemia , relatada por vários autores 28,35 , esteja ligada não só aos níveis plasmáticos de cortisol 36 , mas também à ação das interleucinas e prostaglandinas 37,38. A demonstração de que a infusão combinada de cortisol, insulina e glucagon, por período superior a 3 dias 24 , falha na manutenção da resistência insulínica, é mais uma evidência do papel das citoquinas na gênese da proteólise observada nas primeiras semanas após o TCE. A queda da glicemia ocorre somente após o final da fase de fluxo, hipercatabólica, que se prolonga, por vezes, além do 10º dia após o trauma 19,39 . A correlação entre a resposta adrenérgica, hipermetabólica e a evolução do quadro clínico-metabólico foi discutida por Hörtnagl et al 40 , que demonstraram queda da atividade do sistema nervoso simpático, ao final da fase de transição da fase mesencefálica para a fase apalidal traumática, com recuperação gradual das funções cognitivas.…”